| Structural highlights
Function
CLC2D_MOUSE Receptor for KLRB1B that protects target cells against natural killer cell-mediated lysis (PubMed:14990792, PubMed:16751398). Inhibits osteoclast formation (PubMed:11278931, PubMed:12374791). Binds high molecular weight sulfated glycosaminoglycans (PubMed:15123656).[1] [2] [3] [4] [5]
Publication Abstract from PubMed
The interaction between natural killer (NK) cell inhibitory receptors and their cognate ligands constitutes a key mechanism by which healthy tissues are protected from NK cell-mediated lysis. However, self-ligand recognition remains poorly understood within the prototypical NKR-P1 receptor family. Here we report the structure of the inhibitory NKR-P1B receptor bound to its cognate host ligand, Clr-b. NKR-P1B and Clr-b interact via a head-to-head docking mode through an interface that includes a large array of polar interactions. NKR-P1B:Clr-b recognition is extremely sensitive to mutations at the heterodimeric interface, with most mutations severely impacting both Clr-b binding and NKR-P1B receptor function to implicate a low affinity interaction. Within the structure, two NKR-P1B:Clr-b complexes are cross-linked by a non-classic NKR-P1B homodimer, and the disruption of homodimer formation abrogates Clr-b recognition. These data provide an insight into a fundamental missing-self recognition system and suggest an avidity-based mechanism underpins NKR-P1B receptor function.
Recognition of host Clr-b by the inhibitory NKR-P1B receptor provides a basis for missing-self recognition.,Balaji GR, Aguilar OA, Tanaka M, Shingu-Vazquez MA, Fu Z, Gully BS, Lanier LL, Carlyle JR, Rossjohn J, Berry R Nat Commun. 2018 Nov 5;9(1):4623. doi: 10.1038/s41467-018-06989-2. PMID:30397201[6]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
References
- ↑ Zhou H, Kartsogiannis V, Hu YS, Elliott J, Quinn JM, McKinstry WJ, Gillespie MT, Ng KW. A novel osteoblast-derived C-type lectin that inhibits osteoclast formation. J Biol Chem. 2001 May 4;276(18):14916-23. Epub 2001 Feb 13. PMID:11278931 doi:http://dx.doi.org/10.1074/jbc.M011554200
- ↑ Zhou H, Kartsogiannis V, Quinn JM, Ly C, Gange C, Elliott J, Ng KW, Gillespie MT. Osteoclast inhibitory lectin, a family of new osteoclast inhibitors. J Biol Chem. 2002 Dec 13;277(50):48808-15. Epub 2002 Oct 8. PMID:12374791 doi:http://dx.doi.org/10.1074/jbc.M209059200
- ↑ Carlyle JR, Jamieson AM, Gasser S, Clingan CS, Arase H, Raulet DH. Missing self-recognition of Ocil/Clr-b by inhibitory NKR-P1 natural killer cell receptors. Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3527-32. Epub 2004 Feb 27. PMID:14990792 doi:http://dx.doi.org/10.1073/pnas.0308304101
- ↑ Gange CT, Quinn JM, Zhou H, Kartsogiannis V, Gillespie MT, Ng KW. Characterization of sugar binding by osteoclast inhibitory lectin. J Biol Chem. 2004 Jul 9;279(28):29043-9. Epub 2004 May 3. PMID:15123656 doi:http://dx.doi.org/10.1074/jbc.M312518200
- ↑ Carlyle JR, Mesci A, Ljutic B, Belanger S, Tai LH, Rousselle E, Troke AD, Proteau MF, Makrigiannis AP. Molecular and genetic basis for strain-dependent NK1.1 alloreactivity of mouse NK cells. J Immunol. 2006 Jun 15;176(12):7511-24. PMID:16751398
- ↑ Balaji GR, Aguilar OA, Tanaka M, Shingu-Vazquez MA, Fu Z, Gully BS, Lanier LL, Carlyle JR, Rossjohn J, Berry R. Recognition of host Clr-b by the inhibitory NKR-P1B receptor provides a basis for missing-self recognition. Nat Commun. 2018 Nov 5;9(1):4623. doi: 10.1038/s41467-018-06989-2. PMID:30397201 doi:http://dx.doi.org/10.1038/s41467-018-06989-2
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